The present disclosure relates generally to systems and methods for monitoring nerve activity and, in particular, to systems and methods for non-invasive monitoring and/or controlling nerve activity using cutaneous and/or subcutaneous electrodes.
Many diagnostic and treatment methods in the fields of medicine and biology rely on measurements of nerve activity in patients and test subjects. Nerve activity in humans and other animals generates electrical signals that are detectable by electronic equipment such as oscilloscopes and other electrical signal processing devices. In order to detect the nerve activity, one or more electrical conductors, or electrodes, are placed in proximity to the nerves being measured. The electrodes may receive the electrical signals for further medical analysis. In addition, various medical treatment methods also use electrodes to deliver electrical signals to the nerves in order to induce a response in the patient.
Cardiac care is one particular area of medical treatment that heavily utilizes measurement of nerve activity. Activity in the autonomic nervous system controls the variability of heart rate and blood pressure. The sympathetic and parasympathetic branches of the autonomic nervous system modulate cardiac activity. Elevated levels of sympathetic nerve activity (“SNA”) are known to be correlated with heart failure, coronary artery disease, and may be associated with the initiation of hypertension. SNA is also thought to be important as a predictor of heart rhythm disorders, including sudden cardiac death.
Sympathetic nerve activity measurements have many medical uses including identification of specific conditions or determination of a treatment course. For example, previous studies have shown that directly recorded stellate ganglion nerve activity (“SGNA”) immediately precedes heart rate acceleration and spontaneous cardiac arrhythmias. However, one challenge to measuring nerve activity is that the magnitude of electrical signals in the sympathetic nerves is relatively low, while various other electrical signals present in a patient provide noise that may interfere with isolation and detection of the sympathetic nerve activity. For example, in the human body and the bodies of many animals the electrical activity in the cardiac muscle generates electrical signals with much greater amplitudes than the amplitudes of electrical signals in the nerves. Other muscles in the body can also generate large electrical signals, but the cardiac muscle contractions in a heartbeat occur continuously during any nerve monitoring procedure, and the electrical signals from the cardiac muscle contractions present difficulties in monitoring the lower amplitude signals in the nerve fibers.
In general, sympathetic nerve activity is measured by bringing one or more electrodes into contact with a target nerve that is insulated from the surrounding tissue, and then the grouped action potentials are measured. However, in addition to the fact that measured signals are in microvolts, a number of factors, including differences in contact between the nerve and the electrodes, could lead to differences in the amplitude of the recorded signal. In addition, such procedures are generally invasive in order to gain access to the target nerves. For example, direct recording from the stellate ganglion would necessitate an incision into the pleural space of the chest.
Cardiac sympathetic innervation derives from the paravertebral cervical and thoracic ganglia. In particular, the stellate (cervicothoracic) ganglion is a major source of cardiac sympathetic innervation, formed by the fusion of the inferior cervical ganglion and the first thoracic ganglion. Clinical studies have shown that the left stellate ganglion is an important component in cardiac arrhythmogenesis. Specifically excessive sympathetic outflow from the stellate ganglion is a major cause of heart rhythm problems, and may, in part, account for the pathophysiology of heart failure.
Reducing the sympathetic outflow by stellate ganglion resection has been known to be anti-arrhythmic. In addition, stellate ganglion ablation has also been used as a method for preventing sudden death in patients with life threatening ventricular arrhythmias. However, these approaches generally require surgeons to enter the thoracic cavity of a subject in order to find and destroy the stellate ganglion. As such, need for an invasive procedures has prevented widespread use, and particularly with respect to patients with less than lethal cardiac arrhythmia.
In a previous study, it was found that vagal nerve stimulation can reduce SGNA and control atrial fibrillation. However, the vagal nerve is a vital structure responsible for a variety of functions including heart rate, gastrointestinal peristalsis, sweating, muscle movements, and so on. Gaining access to the vagal nerve requires an expert neurosurgeon or vascular surgeon, and the procedure is considered to be very delicate involving high risk. If the vagal nerve is accidentally damaged, the consequences to the subject body would be severe. As such, several clinical studies involving vagal nerve stimulation have reported a number of serious adverse effects and even death.
Given the above, there is a continuing need for systems and methods capable of monitoring and/or controlling various cardiac and other conditions using limited or non-invasive procedures that minimize risk and complications.